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Endothelial long non-coding RNAs regulated by oxidized LDL.

Krishna K Singh1,2,3,4, Pratiek N Matkar5, Yi Pan6

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This study reveals how oxidized low-density lipoprotein (oxLDL) affects gene expression in human endothelial cells. It identifies numerous long non-coding RNAs (lncRNAs) and mRNAs that change, offering new insights into atherosclerosis development.

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Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Genomics

Background:

  • Oxidized low-density lipoprotein (oxLDL) is implicated in atherosclerosis and endothelial dysfunction.
  • Understanding molecular changes in endothelial cells is crucial for atherosclerosis research.

Purpose of the Study:

  • To profile long non-coding RNA (lncRNA) and messenger RNA (mRNA) expression in human endothelial cells stimulated with oxLDL.
  • To identify novel molecular targets involved in oxLDL-induced endothelial dysfunction and atherogenesis.

Main Methods:

  • Human umbilical vein endothelial cells (HUVECs) were treated with oxLDL (100 µg/mL) for 24 hours.
  • Global lncRNA and mRNA expression profiling was performed using the Arraystar Human lncRNA Expression Microarray V3.0.
  • Differential expression analysis identified significantly altered lncRNAs and mRNAs (P < 0.05).

Main Results:

  • Oxidized low-density lipoprotein (oxLDL) significantly altered the expression of 923 lncRNAs (up-regulated) and 975 lncRNAs (down-regulated).
  • Oxidized low-density lipoprotein (oxLDL) also affected mRNA expression, with 518 up-regulated and 572 down-regulated.
  • Specific lncRNAs, CLDN10-AS1 and CTC-459I6.1, showed substantial fold-change differences.
  • Bioinformatic analysis linked differentially expressed genes to key signaling pathways, including cytokine receptor, chemokine, TNF, MAPK, and Ras pathways.

Conclusions:

  • This is the first study to comprehensively profile oxLDL-induced lncRNA and mRNA expression changes in human endothelial cells.
  • The identified novel lncRNAs and mRNAs represent potential therapeutic targets and biomarkers for atherosclerosis.
  • These findings expand the understanding of molecular mechanisms underlying oxLDL-mediated endothelial dysfunction and atherogenesis.